Age-related macular degeneration (AMD) constitutes a degenerative condition impacting the macula, resulting in the gradual impairment of central visual perception (Coleman et al., 2008). AMD advances through three stages based on the macular appearance: early, intermediate, and late stages (Lim et al., 2012; Mitchell et al., 2018). The condition is classified into two primary types: dry AMD (geographical atrophy, GA) accounting for 85%–90%, and wet AMD (choroidal neovascularization, CNV)(Group et al., 2011). Approximately 8.7% of adults aged 45–85 years suffer from AMD, and it is estimated that this number may rise to nearly 300 million individuals worldwide by the middle of the century (Wong et al., 2014). The early phase of AMD is characterized by the presence of subretinal lesions or drusen, yellowish extracellular deposits of varying sizes found between either the retinal pigment epithelium (RPE) and photoreceptors or RPE and Bruch's membrane (Lim et al., 2012). In a systematic review, researchers identified more than 70 risk factors for advanced AMD, including atherosclerotic heart disease, demographic factors, environmental factors, genetic factors, ocular comorbidities, and personal habits (Chakravarthy et al., 2010). As early as 1979, researchers considered refractive error (RE) as a variable that may increase the risk of AMD development (Maltzman et al., 1979). However, the findings of cross-sectional and prospective studies have been inconsistent throughout the years (Lavanya et al., 2010; Pan et al., 2013; Li et al., 2014; Lin et al., 2016). Moreover, the use of randomized control trials (RCTs) to demonstrate causality for risk factors presents practical and ethical challenges (Keenan et al., 2019; Christen et al., 2020). Mendelian randomization (MR), a recent analytical technique, offers an alternative strategy for inferring causal effects from exposures (Smith and Ebrahim, 2003; Zuccolo and Holmes, 2017). In a Mendelian Randomization approach, the utilization of single nucleotide polymorphisms (SNPs) as instrumental variables (IVs) which are unconfounded enables them to serve as effective proxies for specific phenotypic traits (Hartwig et al., 2016). The random assignment of genetic variants during fertilization makes confounding factors (such as gender or age) less likely to bias causal conclusions, thereby simulating a randomized controlled trial (Burgess et al., 2013). Utilizing genome-wide association study (GWAS) data from large population samples that are publicly available, the present research examines the proposition that refractive error possesses a causal link to early AMD through the application of Mendelian Randomization (MR) methodology.